Functional alterations of cardiac subcellular structures during energy deficiency in relation to the metabolic state of the heart muscle cell

Abstract

The functional behaviour of membrane systems of the cardiac cell during oxygen deficiency was analyzed and the alterations were related to the metabolic state of the tissue as an index of injury. 1. The retention function of the cell membrane for proteins. With increasing energy deficiency the cardiac sarcolemma loses its ability to retain macromolecules (myoglobin, enzymes) within the cell. Close correlations exist between protein release and oxygen supply as well as ATP content of the tissue. 2. Function of isolated mitochondria after ischemia. In parallel with a strong impairment of oxidative phosphorylation (decrease of QO2, RCI values, phosphorylation rates) the Ca++-transporting activity of mitochondria is continuously depressed with decreasing myocardial ATP. 3. Function of isolated sarcoplasmic reticulum after ischemia. With breakdown of high energy phosphates during ischemia rate and extent of Ca++ binding with decrease markedly.

Hearts during ischemia with or without HTK-protection analysed by dielectric spectroscopy

“…The depletion of Ca ++ from the extracellular space by pre-ischemic perfusion with HTK solution in group HTK prohibited the high Ca ++ influx from the extracellular space so that the Ca ++ level cannot cross the trigger threshold needed for gap junction closure before additional Ca ++ is released, probably from the sarcoplasmic reticulum (SR). The SR as a source for additional Ca ++ could also explain the increase in t-in between 15 °C and 5 °C in group HTK (see table 3) because the binding of Ca ++ to the SR depends on ATP concentration (Spieckermann 1980) and on intracellular pH (Krause 1984) and both, ATP depletion and the decrease in intracellular pH, were delayed by deepening hypothermia (see figures 7(b) and 8(b)).…”